miR302 regulates SNAI1 expression to control mesangial cell plasticity View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-02-14

AUTHORS

Letizia De Chiara, Darrell Andrews, Ariane Watson, Giorgio Oliviero, Gerard Cagney, John Crean

ABSTRACT

Cell fate decisions are controlled by the interplay of transcription factors and epigenetic modifiers, which together determine cellular identity. Here we elaborate on the role of miR302 in the regulation of cell plasticity. Overexpression of miR302 effected silencing of the TGFβ type II receptor and facilitated plasticity in a manner distinct from pluripotency, characterized by increased expression of Snail. miR302 overexpressing mesangial cells also exhibited enhanced expression of EZH2 coincident with Snail upregulation. esiRNA silencing of each component suggest that Smad3 and EZH2 are part of a complex that regulates plasticity and that miR302 regulates EZH2 and Snail independently. Subsequent manipulation of miR302 overexpressing cells demonstrated the potential of using this approach for reprogramming as evidenced by de novo expression of the tight junction components ZO-1 and E-cadherin and the formation of ZO-1 containing tight junctions. Understanding the processes through which dynamic epigenetic silencing is controlled in adults cells will allow us to address the epigenetic state of acquired disease and whether original states, regenerative in nature, can be restored with therapy. More... »

PAGES

42407

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/srep42407

DOI

http://dx.doi.org/10.1038/srep42407

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1083820414

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/28195240


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